Effect of orthopedic and functional orthodontic treatment in children with obstructive sleep apnea: A systematic review and meta-analysis.

Orthodontic treatment is suggested in growing individuals to correct transverse maxillary deficiency and mandibular retrusion. Since, as a secondary effect, these orthodontic procedures may improve pediatric obstructive sleep apnea (OSA), this systematic review assessed their effects on apnea-hypopnea index (AHI) and oxygen saturation (SaO2). Twenty-five (25) manuscripts were included for qualitative synthesis, 19 were selected for quantitative synthesis.

Autophagy suppresses the formation of hepatocyte-derived cancer-initiating ductular progenitor cells in the liver.

Hepatocellular carcinoma (HCC) is driven by repeated rounds of inflammation, leading to fibrosis, cirrhosis, and, ultimately, cancer. A critical step in HCC formation is the transition from fibrosis to cirrhosis, which is associated with a change in the liver parenchyma called ductular reaction. Here, we report a genetically engineered mouse model of HCC driven by loss of macroautophagy and hemizygosity of phosphatase and tensin homolog, which develops HCC involving ductular reaction.

mTORC1 Activation Requires DRAM-1 by Facilitating Lysosomal Amino Acid Efflux.

Sensing nutrient availability is essential for appropriate cellular growth, and mTORC1 is a major regulator of this process. Mechanisms causing mTORC1 activation are, however, complex and diverse. We report here an additional important step in the activation of mTORC1, which regulates the efflux of amino acids from lysosomes into the cytoplasm.

Mannose impairs tumour growth and enhances chemotherapy.

It is now well established that tumours undergo changes in cellular metabolism. As this can reveal tumour cell vulnerabilities and because many tumours exhibit enhanced glucose uptake, we have been interested in how tumour cells respond to different forms of sugar. Here we report that the monosaccharide mannose causes growth retardation in several tumour types in vitro, and enhances cell death in response to major forms of chemotherapy.

Parkin-Independent Mitophagy Controls Chemotherapeutic Response in Cancer Cells.

Mitophagy is an evolutionarily conserved process that selectively targets impaired mitochondria for degradation. Defects in mitophagy are often associated with diverse pathologies, including cancer. Because the main known regulators of mitophagy are frequently inactivated in cancer cells, the mechanisms that regulate mitophagy in cancer cells are not fully understood.

Low carbohydrate diet prevents Mcl-1-mediated resistance to BH3-mimetics.

Overexpression of Mcl-1 is implicated in resistance of several cancers to chemotherapeutic treatment, therefore identifying a safe way to decrease its expression in tumor cells represents a central goal. We investigated if a modulation of the diet could impact on Mcl-1 expression using a Myc-driven lymphoma model. We established that a partial reduction of caloric intake by 25% represents an efficient way to decrease Mcl-1 expression in tumor cells.

Hyperthermic intra-peritoneal chemotherapy and anticancer immune response.

Peritoneal carcinomatosis (PC) is a metastatic disease of primary tumors localized in the abdomen. Although this disease is considered a terminal condition, recent treatments combining surgery with heated intra-peritoneal chemotherapy (HIPEC) significantly increase patient survival. We have determined that the protective effect of HIPEC is partially linked to the induction of an efficient anticancer immune response.

In-situ photo-assisted deposition of silver particles on hydrogel fibers for antibacterial applications.

Silver nanoparticles (AgNPs) have attracted intensive research interest and have been recently incorporated in polymers, medical devices, hydrogels and burn dressings to control the proliferation of microorganisms. In this study a novel silver antibacterial coating was deposited for the first time on hydrogel fibers through an in-situ photo-chemical reaction. Hydrogel blends obtained by mixing different percentages of silver-treated and untreated fibers were characterized by thermogravimetric analysis (TGA), Fourier transform infrared spectroscopy (FT-IR), scanning electron microscopy (SEM) and energy dispersive X-ray spectroscopy (EDX).

Hyperthermic intraperitoneal chemotherapy leads to an anticancer immune response via exposure of cell surface heat shock protein 90.

The occurrence of peritoneal carcinomatosis is a major cause of treatment failure in colorectal cancer and is considered incurable. However, new therapeutic approaches have been proposed, including cytoreductive surgery combined with hyperthermic intraperitoneal chemotherapy (HIPEC). Although HIPEC has been effective in selected patients, it is not known how HIPEC prolongs a patient's lifespan.

GAPDH enhances the aggressiveness and the vascularization of non-Hodgkin's B lymphomas via NF-κB-dependent induction of HIF-1α.

Deregulated expression of glycolytic enzymes contributes not only to the increased energy demands of transformed cells but also has non-glycolytic roles in tumors. However, the contribution of these non-glycolytic functions in tumor progression remains poorly defined. Here, we show that elevated expression of glyceraldehyde-3-phosphate dehydrogenase (GAPDH), but not of other glycolytic enzymes tested, increased aggressiveness and vascularization of non-Hodgkin's lymphoma.

Glucose metabolism is inhibited by caspases upon the induction of apoptosis.

Rapidly proliferating cells, such as cancer cells, have adopted aerobic glycolysis rather than oxidative phosphorylation to supply their energy demand; this phenomenon is known as 'the Warburg effect'. It is now widely accepted that during apoptosis the loss of energy production, orchestrated by caspases, contributes to the dismantling of the dying cell. However, how this loss of energy production occurs is still only partially known.

Caloric restriction modulates Mcl-1 expression and sensitizes lymphomas to BH3 mimetic in mice.

Caloric restriction (CR) is proposed to decrease tumorigenesis through a variety of mechanisms including effects on glycolysis. However, the understanding of how CR affects the response to cancer therapy is still rudimentary. Here, using the Eµ-Myc transgenic mouse model of B-cell lymphoma, we report that by reducing protein translation, CR can reduce expression of the prosurvival Bcl-2 family member Mcl-1 and sensitize lymphomas to ABT-737-induced death in vivo.

GAPDH binds to active Akt, leading to Bcl-xL increase and escape from caspase-independent cell death.

Increased glucose catabolism and resistance to cell death are hallmarks of cancers, but the link between them remains elusive. Remarkably, under conditions where caspases are inhibited, the process of cell death is delayed but rarely blocked, leading to the occurrence of caspase-independent cell death (CICD). Escape from CICD is particularly relevant in the context of cancer as apoptosis inhibition only is often not sufficient to allow oncogenic transformation.

Combination of glycolysis inhibition with chemotherapy results in an antitumor immune response.

Most DNA-damaging agents are weak inducers of an anticancer immune response. Increased glycolysis is one of the best-described hallmarks of tumor cells; therefore, we investigated the impact of glycolysis inhibition, using 2-deoxyglucose (2DG), in combination with cytotoxic agents on the induction of immunogenic cell death. We demonstrated that 2DG synergized with etoposide-induced cytotoxicity and significantly increased the life span of immunocompetent mice but not immunodeficient mice.